The juxtaposition of changes in brain structure/function and ADHD behavior from adolescence to adulthood raises the possibility that the two might be linked. Furthermore, if these factors are directly related, a link should be observable in a study that focuses on a core impairment of ADHD (i.e., response inhibition) across different age groups. Two positions have arisen in the field of developmental neurobiology to explain how ADHD symptoms diminish. First, some researchers hold that brain areas crucial for behavioral inhibition (i.e., ventral prefrontal cortex) may continue to mature, albeit at a delay. Second, it is possible that other, unimpaired cognitive mechanisms develop to compensate for behavioral inhibition system impairment. Among others, some candidate compensatory mechanisms include stimulus evaluation or working memory processes. Because of the lack of research, neither of these positions have great support at the current time; moreover, the two possibilities are not incompatible. However, this question is crucial in understanding the pathophysiology of ADHD. Figure 2 (right) depicts a two possible relationships of response inhibition development in terms of ERP N2 amplitude. In Figure 2A, the diminished N2 seen in ADHD youth could be hypothesized to resolve with increasing age. Alternatively (Figure 2B), there may be no such gains in response inhibition N2 neural function. Rather, other cognitive processes that can be measured with different ERP indices may reflect the development of compensatory neural mechanisms in older ADHD persons, such as those reflected by the P3.